ライフサイエンスコーパス: DNA methyltransferase

1 in heme biogenesis or to function as adenine DNA methyltransferase.

2 n turn, upregulates and activates the DNMT3b DNA methyltransferase.

3 ain 26695, encodes a N(6)-adenosine type III DNA methyltransferase.

4 n DNA methyltransferase (DNMT) 3B, a de novo DNA methyltransferase.

5 clease cleavage by modifying the DNA using a DNA methyltransferase.

6 atalase did not block its ability to inhibit DNA methyltransferase.

7 at undergo CHH methylation via two different DNA methyltransferases.

8 ble 5mC, as well as homologs of the cytosine DNA methyltransferases.

9 hen mediating the recruitment of histone and DNA methyltransferases.

10 f epigenetically silenced genes by targeting DNA methyltransferases.

11 ely expressed or phase variable CpG-specific DNA methyltransferases.

12 modeling, nucleosomes are strong barriers to DNA methyltransferases.

13 independent of the CHROMOMETHYLASE (CMT)2/3 DNA methyltransferases.

14 s study has demonstrated an up-regulation of DNA methyltransferase 1 (DNMT1) and a global hypermethyl

15 on-determining region [G1MDR]) that recruits DNA methyltransferase 1 (Dnmt1) and provokes methylation

16 tical for gene expression, are replicated by DNA methyltransferase 1 (DNMT1) and ubiquitin-like conta

17 gies, we define not only a dominant role for DNA methyltransferase 1 (DNMT1) but also distinct roles

18 Here we show that endogenous DNA methyltransferase 1 (DNMT1) co-purifies with inhibit

19 ce that HFD-fed rats show increased vascular DNA methyltransferase 1 (DNMT1) expression and that HS p

20 ith PHD and ring finger domains 1 (uhrf1) or DNA methyltransferase 1 (dnmt1) genes exhibit a robust i

21 gest that noncytotoxic concentrations of the DNA methyltransferase 1 (DNMT1) inhibitor decitabine pro

22 DNA methyltransferase 1 (DNMT1) is an essential regulato

23 Silencing of tumor-suppressor genes by DNA methyltransferase 1 (Dnmt1) is essential for oncogen

24 Human DNA methyltransferase 1 (DNMT1) maintains the epigenetic

25 The decreased hippocampal expression of DNA methyltransferase 1 (Dnmt1) that maintains the impri

26 chanistically, Naa10p facilitates binding of DNA methyltransferase 1 (Dnmt1) to DNA substrates, inclu

27 Human DNA methyltransferase 1 (Dnmt1), a 1616-amino acid multi

28 The overexpression of four genes, DNA methyltransferase 1 (DNMT1), delta-opioid receptor (

29 ied according to genotype for 11 SNPs within DNA methyltransferase 1 (DNMT1), DNA methyltransferase 3

30 e H3 lysine 27 trimethylation (H3K27me3) and DNA methyltransferase 1 (DNMT1)-mediated DNA methylation

31 igenetically silenced from infancy onward by DNA methyltransferase 1 (DNMT1).

32 am substrate of NPM-ALK, in cooperation with DNA methyltransferase 1 (DNMT1).

33 essential for maintenance DNA methylation by DNA methyltransferase 1 (DNMT1).

34 exts ((m) = methylated) and is maintained by DNA METHYLTRANSFERASE 1 (MET1) and CHROMOMETHYLASE (CMT)

35 Consistent with this model, mutation of DNA METHYLTRANSFERASE 1 (MET1) causes loss of DNA methyl

36 s) in DECREASED DNA METHYLATION 1 (ddm1) and DNA METHYLTRANSFERASE 1 (met1) mutants, as well as in th

37 This includes a significant increase in DNA methyltransferase 1 and ten-eleven-translocation hyd

38 by site-alpha and TATA box, reversible after DNA methyltransferase 1 depletion.

39 4-3-3sigma gene appears to be carried out by DNA methyltransferase 1 under regulation by Uhrf1.

40 DNMT1 (DNA methyltransferase 1) is responsible for propagating

41 in conjunction with CG methylation by MET1 (DNA METHYLTRANSFERASE 1), CHG methylation by CMT3 (CHROM

42 f key chromatin remodeling factors including DNA methyltransferase 1, ten-eleven-translocation hydrox

43 h cover the surface of the omentum, caused a DNA methyltransferase 1-mediated decrease in the express

44 cetylation of histones and downregulation of DNA methyltransferase 1.

45 ted with reduced activity of the E2F target, DNA methyltransferase 1.

46 DNA demethylation in cells disrupted for the DNA methyltransferases 1 and 3B (DNMT1 and 3B) or by DNM

47 rations (DNA methyltransferase-3a [DNMT-3a]; DNA methyltransferase-1 [DNMT-1]; 5-methylcytosine [5-mC

48 global hypermethylation and up-regulation of DNA methyltransferase-1 and -3a.

49 ine, a demethylation agent, and knockdown of DNA methyltransferase-1 partially rescued miR-184 level.

50 egative feedback loop in which SET9 controls DNA methyltransferase-1 protein stability, which repress

51 In addition, DNA methyltransferase-1 was recruited to the promoter re

52 We also show that knocking down DNA methyltransferase 1a (Dnmt1a), Dnmt3, or blocking DN

53 embryo are dependent on the oocyte-specific DNA methyltransferase 1o (DNMT1o), levels of which are d

54 SNPs within DNA methyltransferase 1 (DNMT1), DNA methyltransferase 3 Beta (DNMT3B), Tet methylcytosin

55 tic regulators that lack enzymatic activity, DNA methyltransferase 3-like (DNMT3L) and tripartite mot

56 DNA methyltransferase 3-like (DNMT3L) is an epigenetic r

57 ng multiple copies of antibody-fused de novo DNA methyltransferase 3A (DNMT3A) (dCas9-SunTag-DNMT3A)

58 Abundance of DNA methyltransferase 3a (Dnmt3a) and its interaction wi

59 Mutations in DNA methyltransferase 3A (DNMT3A) are common in acute my

60 DNA methyltransferase 3A (DNMT3A) catalyzes cytosine met

61 novo during neuronal maturation and requires DNA methyltransferase 3A (DNMT3A) for active maintenance

62 Despite a recognized role of DNA methyltransferase 3a (DNMT3a) in human cancer, the n

63 To investigate the role of de novo DNA methyltransferase 3a (Dnmt3a) in intestinal tumor de

64 Here, we demonstrate that DNA methyltransferase 3a (Dnmt3a) is both necessary and

65 DNA methyltransferase 3A (DNMT3A) is frequently mutated

66 The gene that encodes de novo DNA methyltransferase 3A (DNMT3A) is frequently mutated

67 DNA methyltransferase 3A (DNMT3A) is mutated in hematolo

68 We show that DNA methyltransferase 3a (DNMT3a) methylates and silence

69 reduction in medial prefrontal cortex (mPFC)-DNA methyltransferase 3a (Dnmt3a) mRNA levels and a subs

70 ke behavior is accompanied by a reduction in DNA methyltransferase 3a (Dnmt3a) mRNA levels and global

71 Consistent with miR-29's role in targeting DNA methyltransferase 3A (DNMT3A), a key enzyme regulati

72 (HDAC1), SET domain, bifurcated 1 (SETDB1), DNA methyltransferase 3A (DNMT3A), and tripartite motif-

73 Recurrent somatic mutations in DNA methyltransferase 3A (DNMT3A), most frequently at ar

74 which is then followed by the recruitment of DNA methyltransferase 3a (DNMT3a), ultimately resulting

75 cytosine and become eroded in the absence of DNA methyltransferase 3a (Dnmt3a).

76 ugh a six zinc finger (ZF) protein linked to DNA methyltransferase 3A (ZF-DNMT3A).

77 Knockdown of DNA methyltransferase 3a alters gene expression and inhi

78 Furthermore, upregulation of DNA methyltransferase 3a and 3b and global DNA hypomethy

79 ion were apparent in decreased expression of DNA methyltransferase 3a and methyl-5'-cytosine-phosphod

80 periments on mice show that an enzyme called DNA methyltransferase 3a is involved in insulin resistan

81 DNMT3A, the gene encoding the de novo DNA methyltransferase 3A, is among the most frequently m

82 P)-9 expression, and epigenetic alterations (DNA methyltransferase-3a [DNMT-3a]; DNA methyltransferas

83 NA hypermethylation due to overexpression of DNA methyltransferase 3b (and hyperactivity of the DNA m

84 This process is dependent on DNA methyltransferase 3B (DNMT3B) and leads to suppressi

85 Here, we show that heterozygous mutations in DNA methyltransferase 3B (DNMT3B) are a likely cause of

86 Here we show that DNA methyltransferase 3B (DNMT3B) is responsible for the

87 f short hairpin RNA in ESC demonstrated that DNA methyltransferase 3b (Dnmt3b) was responsible for me

88 on through the transcription factor PU.1 and DNA methyltransferase 3b (Dnmt3b).

89 xplained by mutations in the known ICF genes DNA methyltransferase 3B or zinc-finger and BTB domain c

90 DNA methyltransferase 3b overexpression occurs secondary

91 The resulting hyperactivity of DNA methyltransferase 3b produces concurrent DNA methyla

92 H19 knockdown activates SAHH, enabling DNA methyltransferase 3B to methylate a subset of genes.

93 equired to promote stable association of the DNA methyltransferase 3b with the repeat locus.

94 n, or via enforced expression of the de novo DNA methyltransferase 3b.

95 Here, we show that DNA methyltransferase 3bb.1 (dnmt3bb.1) is essential for

96 The role of abnormal DNA methyltransferase activity in the development and pr

97 The minor groove binding hairpin 3 inhibits DNA methyltransferase activity in the major groove at it

98 we explore the novel approach of inhibiting DNA methyltransferase activity using 5-azacytidine (Aza;

99 Dnmt3b was not affected by oxidative stress, DNA methyltransferase activity was increased.

100 methylation, which correlates with increased DNA methyltransferase activity, disruption of adenosine

101 DNA methyltransferase and histone deacetylase inhibitors

102 el of EOC, that clinically relevant doses of DNA methyltransferase and histone deacetylase inhibitors

103 mechanisms of action have been proposed for DNA methyltransferase and histone deacetylase inhibitors

104 ation of a single gene (modA) that encodes a DNA methyltransferase and results in two phenotypically

105 of Naegleria encodes homologues of mammalian DNA methyltransferase and Tet proteins.

106 known how the dynamic activities of cytosine DNA methyltransferases and 5-methylcytosine DNA glycosyl

107 ethylation is antagonistically controlled by DNA methyltransferases and DNA demethylases.

108 DNA methyltransferases and erythropoietin hypermethylati

109 tly, we examined the expression of candidate DNA methyltransferases and found three, DMT1a, DMT1b, an

110 how self-reinforcing feedback loops between DNA methyltransferases and histone modifications charact

111 hat extra-coding RNAs (ecRNAs) interact with DNA methyltransferases and regulate neuronal DNA methyla

112 ack of DNA methylation allows the binding of DNA methyltransferases and repressing proteins, such as

113 fects, in part through the downregulation of DNA methyltransferases and their cofactors.

114 MGMT (O(6)-methylguanine DNA methyltransferase) and APNG (alkylpurine-DNA-N-glyco

115 NA methyltransferase, the Mettl4 (adenine-6) DNA methyltransferase, and the Tet DNA demethylase.

116 At the same time, DNA methyltransferases are upregulated, leading to eleva

117 mutations in DNMT3A, which encodes a de novo DNA methyltransferase, are found in approximately 30% of

118 reciprocal targeting of protein kinases and DNA methyltransferases as an essential strategy for dura

119 ether, these data provide novel evidence for DNA methyltransferases as potential therapeutic targets

120 tion mechanisms can be different in other N6-DNA-methyltransferases, as determined from the explorati

121 We now present evidence that the DNA methyltransferase-associated protein (DMAP) interact

122 Here, we focus on DNA methyltransferase-associated protein 1 (DMAP1), whic

123 te that the two Notch repeat modules and the DNA methyltransferase-associated protein interaction dom

124 This failed to reveal any known (cytosine-5) DNA methyltransferases, but identified homologues for th

125 f the highly conserved and usually essential DNA methyltransferase CcrM.

126 JMJ24 directly targets a DNA methyltransferase, CHROMOMETHYLASE 3 (CMT3), for pro

127 mark through a self-reinforcing loop between DNA methyltransferase CHROMOMETHYLASE3 (CMT3) and H3K9 h

128 uding a major trans-association close to the DNA methyltransferase CMT2.

129 coding the histone methyltransferase KYP and DNA methyltransferase CMT3.

130 methods to uncover the functions of CcrM, a DNA methyltransferase conserved in most Alphaproteobacte

131 l lines to small-molecule inhibitors against DNA methyltransferases (DAC), histone deacetylases (Deps

132 y a DNA demethylase, NMAD-1, and a potential DNA methyltransferase, DAMT-1, which regulate 6mA levels

133 enetic modifiers, including the inhibitor of DNA methyltransferase decitabine as well as the inhibito

134 Genetic analysis of DNA methyltransferase deletion mutants also indicated th

135 es genome-wide DNA methylation patterns in a DNA methyltransferase-dependent (DNMT-dependent) manner.

136 e localization and catalytic activity of the DNA methyltransferase DIM-2.

137 c modification in plant genomes, mediated by DNA methyltransferases (DMTs).

138 Since 5hmC is recognized poorly by DNA methyltransferases, DNA methylation may be lost at 5

139 PAF suppressed the expression of DNA methyltransferase (DNMT) 1 and 3b.

140 altered mRNA levels of epigenetic regulators DNA methyltransferase (DNMT) 1 and DNMT3A in the juvenil

141 f the CD8 cluster through the recruitment of DNA methyltransferase (DNMT) 3a and histone methyltransf

142 e in histone H3 lysine 27 trimethylation and DNA methyltransferase (Dnmt) 3a association with STAT4 t

143 rare genetic disease caused by mutations in DNA methyltransferase (DNMT) 3B, a de novo DNA methyltra

144 preoptic area (POA) is to reduce activity of DNA methyltransferase (Dnmt) enzymes, thereby decreasing

145 transcription; the effects were mitigated by DNA methyltransferase (DNMT) inhibitors and knockdown of

146 ere to determine whether (1) TDCIPP inhibits DNA methyltransferase (DNMT) within embryonic nuclear ex

147 Furthermore, we find that inhibition of DNA methyltransferase (DNMT), whether during training or

148 ind the Polycomb group protein SUZ12 and the DNA methyltransferase (DNMT)3b preferentially in undiffe

149 DNA methyltransferases (DNMT) are promising drug targets

150 hIP) analysis demonstrated that BRCA1, EZH2, DNA methyltransferases (DNMT)1/3a/3b and H3K27me3 are re

151 The maintenance cytosine DNA methyltransferase DNMT1 and de novo methyltransferas

152 and PKC412(R) displayed the up-regulation of DNA methyltransferase DNMT1 and tyrosine-protein kinase

153 d a subset of lncRNAs that interact with the DNA methyltransferase DNMT1 in a colon cancer cell line,

154 ast in part from increased expression of the DNA methyltransferase DNMT1 in WDLS/DDLS.

155 models, we found that downregulation of the DNA methyltransferase DNMT1 induced by the brain microen

156 The DNA methyltransferase Dnmt1 maintains DNA methylation pa

157 Silencing the expression of DNA methyltransferase DNMT1, -2, -3A, and -3B alone by s

158 uits a corepressor complex that includes the DNA methyltransferase DNMT1, resulting in DNA hypermethy

159 moted autophagy-dependent degradation of the DNA methyltransferase DNMT1.

160 ained JAK1/STAT3 signalling is maintained by DNA methyltransferase DNMT1.

161 gate whether 5-aza-2'-deoxycytidine (Aza), a DNA methyltransferase (DNMT1) inhibitor, reduces high bl

162 1E) and a potential pathogenic mechanism for DNA methyltransferase (DNMT1) mutations.

163 novo DNA methylation by catalytically active DNA methyltransferases (DNMT1 and DNMT3A/B) require acce

164 l signaling and transcription, including the DNA methyltransferase, DNMT1.

165 iption, we conditionally disrupted two major DNA methyltransferases, Dnmt1 or Dnmt3a, in fetal and ad

166 ally increased the expression of the de novo DNA methyltransferase Dnmt3a [DNA (cytosine-5-)-methyltr

167 ng the ATRX-DNMT3-DNMT3L (ADD) domain of the DNA methyltransferase Dnmt3a as a paradigm, we apply pro

168 that is mediated by induction of the de novo DNA methyltransferase DNMT3A during the first weeks afte

169 The DNA methyltransferase Dnmt3a has high expression in term

170 ral nerve injury increases expression of the DNA methyltransferase DNMT3a in the injured DRG neurons

171 hown that during postnatal life, the de novo DNA methyltransferase DNMT3A initiates a metabolic progr

172 The de novo DNA methyltransferase Dnmt3a is implicated in this proce

173 Furthermore, knockdown of DNA methyltransferase DNMT3A markedly enhanced rDNA tran

174 Recently, we reported that loss of de novo DNA methyltransferase Dnmt3a results in HSC expansion an

175 The DNA methyltransferase Dnmt3a suppresses tumorigenesis in

176 (dCas9) nuclease and catalytic domain of the DNA methyltransferase DNMT3A targeted by co-expression o

177 how that in the brain during early life, the DNA methyltransferase DNMT3A transiently binds across tr

178 In this work, we employed a DNA methyltransferase Dnmt3a-Dnmt3L construct fused to t

179 y in myeloid diseases, including the de novo DNA methyltransferase DNMT3A.

180 The de novo DNA methyltransferases Dnmt3a and Dnmt3b are of crucial

181 The DNA methyltransferases DNMT3A and DNMT3B are primarily r

182 016) find an unexpected role for the de novo DNA methyltransferases Dnmt3a and Dnmt3b in the regulati

183 p53 restricts the expression of the de novo DNA methyltransferases Dnmt3a and Dnmt3b while up-regula

184 ethylation patterns are initiated by de novo DNA methyltransferases DNMT3a/3b adding methyl groups to

185 Recent evidence associating the de novo DNA methyltransferase Dnmt3b with H3K36me3-rich chromati

186 7 putative tumor suppressor genes, including DNA methyltransferase Dnmt3b, in Dnmt3a-deficient lympho

187 licase DNA-binding protein 8 (CHD8), and the DNA methyltransferase DNMT3B, resulting in hypermethylat

188 he chromatin remodeling factor CHD8, and the DNA methyltransferase DNMT3B, resulting in hypermethylat

189 Hypomorphic mutations in DNA-methyltransferase DNMT3B cause majority of the rare

190 Aberrant expression of the DNA methyltransferases (DNMTs) and disruption of DNA met

191 based on DNA damage-related binding between DNA methyltransferases (DNMTs) and PARP1.

192 respective modifying enzymes G9a, EZH2, and DNA methyltransferases (Dnmts) and respective binding pr

193 Although DNA methyltransferases (DNMTs) are dispensable for embry

194 DNA methyltransferases (DNMTs) are important enzymes inv

195 thyl-CpG-binding domain protein 2 (MBD2) and DNA methyltransferases (DNMTs) at the leptin promoter ar

196 establishment and maintenance activities of DNA methyltransferases (DNMTs) can help in the developme

197 yonic stem cells (mESCs) lacking the de novo DNA methyltransferases (Dnmts) Dnmt3a and Dnmt3b.

198 rant DNAm during OS through interacting with DNA methyltransferases (DNMTs) in a "Yin-Yang" complex t

199 caffeine exposure causes down-regulation of DNA methyltransferases (DNMTs) in embryonic heart and re

200 e inactivated all three catalytically active DNA methyltransferases (DNMTs) in human embryonic stem c

201 Despite the abundance of DNA methyltransferases (Dnmts) in the brain, which are r

202 ssociated gene silencing, through inhibiting DNA methyltransferases (DNMTs) is an important potential

203 ene loci by conjugating catalytic domains of DNA methyltransferases (DNMTs) to engineered transcripti

204 ed drug screen, we report that inhibitors of DNA methyltransferases (DNMTs), decitabine and FdCyd, bl

205 Because DNA methylation is reversible, the DNA methyltransferases (DNMTs), responsible for this epi

206 fications, including cytosine methylation by DNA methyltransferases (DNMTs).

207 nal implication in balancing the activity of DNA methyltransferases (DNMTs).

208 hysically associated with both viral DNA and DNA methyltransferases (DNMTs).

209 rentiation and is mediated by the actions of DNA methyltransferases (DNMTs).

210 We further found that the de novo DNA methyltransferase DOMAINS REARRANGED METHYLTRANSFERA

211 t-specific RNA polymerase V with the de novo DNA methyltransferase DRM2.

212 ion of SDCpro-GFP, redundantly controlled by DNA methyltransferases DRM2 and CMT3.

213 lighted by the dynamic expression of de novo DNA methyltransferases during the perinatal period and n

214 , where an inactive form of Cas9 is fused to DNA methyltransferase effectors.

215 DNA methylation and specifically the DNA methyltransferase enzyme DNMT3A are involved in the

216 creased activity of a potentially regulatory DNA methyltransferase enzyme.

217 thyltransferase 3b (and hyperactivity of the DNA methyltransferase enzymes).

218 hed at the exit from pluripotency by de novo DNA methyltransferases enzymes, DNMT3A and DNMT3B, which

219 DNMT3A encodes a DNA methyltransferase essential for establishing methyla

220 DNMT3a is a de novo DNA methyltransferase expressed robustly after T-cell ac

221 d that this change correlates with decreased DNA methyltransferase expression in the same cell popula

222 quently present and catalyzed by a different DNA methyltransferase family, Dnmt5.

223 DAC CSC, and we determined the importance of DNA methyltransferases for CSC maintenance and tumorigen

224 M.TaqI is a DNA methyltransferase from Thermus aquaticus that cataly

225 d further yielded a novel association in the DNA methyltransferase gene DNMT3B.

226 lone, with consideration of O6-methylguanine-DNA-methyltransferase gene (MGMT) promoter methylation s

227 elated to liver injury, levels of SAHH, SAH, DNA methyltransferases genes (Dnmt1, Dnmt3a, Dnmt3b), an

228 The Dnmt3a DNA methyltransferase has been shown to bind cooperative

229 pression of these genes by inhibition of the DNA methyltransferases has been successful in the treatm

230 ctions, chromatin-modifying enzymes (such as DNA methyltransferase, histone deacetylases, and lysine-

231 at observed for germ cells deficient for the DNA methyltransferase homologue DNMT3L.

232 se transgenic knockout of Tgbr2 had elevated DNA methyltransferase I (DNMT1) activity and histone H3

233 ranscription, as transcription is reduced in DNA methyltransferase I (Dnmt1) knockout embryonic stem

234 The only known DNA methyltransferase in Drosophila is the DNMT2 homolog

235 Dali interacts with the DNMT1 DNA methyltransferase in mouse and human and regulates D

236 CMTs are evolutionary conserved DNA methyltransferases in Viridiplantae.

237 1 pathway as a determinant of sensitivity to DNA methyltransferase inhibition, specifically implicati

238 We used the established DNA methyltransferase inhibitor (DNMTi) 5-aza-deoxycitid

239 ncreased after treatment of the cells with a DNA methyltransferase inhibitor (R = 0.6, P = 2.8 x 10(-

240 Furthermore, intra-NAc injections of a DNA methyltransferase inhibitor (RG108, 100 mum) abolish

241 and function of regulatory T cells using the DNA methyltransferase inhibitor 5-azacytidine (Aza).

242 ian cancer who received carboplatin plus the DNA methyltransferase inhibitor guadecitabine or a stand

243 Infusion of the DNA methyltransferase inhibitor RG108 prevented both esc

244 Treatment with the DNA methyltransferase inhibitor Zebularine increases miR

245 tized the screen by "priming" cells with the DNA methyltransferase inhibitor, 5-aza-2'-deoxycytidine

246 Treatment with the DNA methyltransferase inhibitor, decitabine, restored ex

247 When these cells were treated with DNA methyltransferase inhibitor, TLR2 mRNA and cytokine

248 the 2D-cultured HMEC after treatment with a DNA methyltransferase inhibitor.

249 utcomes of patients who are coadministered a DNA methyltransferase inhibitor.

250 DNA methyltransferase inhibitors (DMTis) are used to tre

251 w stroma in regulating clinical responses to DNA methyltransferase inhibitors (DNMTi) is also poorly

252 how this deficiency may influence the use of DNA methyltransferase inhibitors (DNMTis) for treatment

253 We show that DNA methyltransferase inhibitors (DNMTis) upregulate imm

254 Combining DNA-demethylating agents (DNA methyltransferase inhibitors [DNMTis]) with histone

255 Overall, our results demonstrated that DNA methyltransferase inhibitors preferentially target c

256 sions induced by reactive oxygen species and DNA methyltransferase inhibitors was examined.

257 as shown that epigenetic drugs, specifically DNA methyltransferase inhibitors, can upregulate immune

258 te recognized by these Type III N(6)-adenine DNA methyltransferases is not known.

259 rhoeae FA1090 are composed of three genes: a DNA methyltransferase (M.CglI and M.NgoAVII), a putative

260 th factor or unmethylated O(6)-methylguanine-DNA methyltransferase may benefit from Ona + Bev.

261 d miR-205 transcription by the inhibition of DNA methyltransferase-mediated DNA methylation of the mi

262 or size, resection extent, O-6-methylguanine-DNA methyltransferase-methylation, and isocitrate dehydr

263 in addition to changes in O(6)-methylguanine DNA methyltransferase (MGMT) activity, small changes in

264 TMZ-induced DNA damage by O-6-methylguanine-DNA methyltransferase (MGMT) confers one mechanism of TM

265 O(6)-Methylguanine-DNA methyltransferase (MGMT) is a DNA repair enzyme that

266 The DNA repair enzyme O6-methylguanine-DNA methyltransferase (MGMT) is commonly overexpressed i

267 promoter methylation of O (6)-methylguanine-DNA methyltransferase (MGMT) remains controversial for b

268 status of the promoter of O(6)-methylguanine-DNA methyltransferase (MGMT) was assessed.

269 the targeted knockdown of O(6)-methylguanine-DNA methyltransferase (MGMT), a DNA repair protein invol

270 thyltransferases, chiefly O(6)-methylguanine-DNA methyltransferase (MGMT), a key enzyme for resistanc

271 different proteins, avidin, O6-methylguanine DNA methyltransferase (MGMT), SNAP-tag, and lactoferrin,

272 the cytotoxic response of O(6)-methylguanine-DNA methyltransferase (MGMT)-deficient mammalian cells a

273 to the DNA repair protein O(6)-methylguanine-DNA-methyltransferase (MGMT).

274 Phase variably expressed N(6)-adenine DNA methyltransferases (Mod) alter global methylation pa

275 Three phase variable DNA methyltransferases (ModA, ModB and ModD), which medi

276 mophilus influenzae contains an N(6)-adenine DNA-methyltransferase (ModA) that is subject to phase-va

277 Here, we characterize a phase-variable DNA methyltransferase (ModM), which contains 5'-CAAC-3'

278 Cas9 (dCas9) with an engineered prokaryotic DNA methyltransferase MQ1.

279 tection of DNA methylation, determination of DNA methyltransferase (MTase) activity and screening of

280 simple and highly sensitive electrochemical DNA methyltransferase (MTase) activity assay is presente

281 Bio sequencing, the recognition sequences of DNA methyltransferases (MTases) are appearing rapidly.

282 S-Adenosylmethionine-dependent DNA methyltransferases (MTases) perform direct methylati

283 The advent of engineered DNA methyltransferases (MTases) to target DNA methylatio

284 It is catalyzed by DNA methyltransferases, one of which -DNMT3A- is frequen

285 Of all known DNA methyltransferases, only CHROMOMETHYLASE 3 (CMT3) is

286 A P16-specific DNA methyltransferase (P16-dnmt) expression vector is de

287 the factors age, WHO grade, O6-methylguanine-DNA methyltransferase promoter methylation status, contr

288 hepatocyte growth factor, O(6)-methylguanine-DNA methyltransferase promoter methylation, and glioblas

289 t harbors a nonmethylated O(6)-methylguanine-DNA methyltransferase promotor, standard temozolomide (T

290 ANSFERASE 1 (MET1) and CHROMOMETHYLASE (CMT) DNA methyltransferase protein families, respectively.

291 ably targets CTCF binding at the promoter of DNA methyltransferases, regulating their expression.

292 f chromatin folding that restricts access to DNA methyltransferases responsible for gene body methyla

293 of covalent attachment to O(6)-methylguanine DNA methyltransferase (SNAP-tag) fusion proteins.

294 gnificance, with WHO grade, O6-methylguanine-DNA methyltransferase status, age, and TTP(min) remainin

295 Plants encode a diverse repertoire of DNA methyltransferases that have specialized to target c

296 e findings reveal how CTCF binding regulates DNA methyltransferase to reprogram the methylome in resp

297 ed whether lncRNAs could also associate with DNA methyltransferases to regulate DNA methylation and g

298 Our results show that mRNA levels of DNA methyltransferase were increased in demyelinated MS

299 ins to sites of DNA damage repair, including DNA methyltransferases where it imposes de novo DNA meth

300 We have identified a highly conserved DNA methyltransferase, which we term Campylobacter trans